BIN1 Mouse Monoclonal Antibody [Clone ID: 12A]

Specifications

Product Data
Clone Name	12A
Applications	WB
Recommend Dilution	ELISA: 1:5000-1:50000, WB: 1:500-1:1500
Reactivity	Human
Host	Mouse
Clonality	Monoclonal
Immunogen	Anti-BIN1 (MOUSE) Monoclonal Antibody was produced in mouse by repeated immunizations with 12A exon BIN1 protein followed by hybridoma development.
Formulation	0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2
Concentration	lot specific
Conjugation	Unconjugated
Storage Condition	Store at -20°C as received.
Gene Name	bridging integrator 1
Database Link	NP_004296 Entrez Gene 274 Human UniProt ID O00499
Synonyms	AMPH2; AMPHL; SH3P9
Note	Bin1 is a conserved member of the BAR family of genes that have been implicated in diverse cellular processes including endocytosis, actin organization, programmed cell death, stress responses, and transcriptional control. The first mammalian BAR protein to be discovered, Amphiphysin I (AmphI), was identified in an immunoscreen for proteins associated with the plasma membranes of synaptic neurons, functions in the control of clathrin-dependent synaptic vesicle endocytosis. The mammalian Bin1 gene was first identified in a two hybrid screen for polypeptides that bind to the N-terminal Myc box 1 (MB1) portion of the c-Myc oncoprotein. Bin1 is similar to AmphI in overall structure, with an N-terminal BAR domain and a C-terminal SH3 domain. However, the Bin1 gene is more complex than the AmphI gene, encoding at least seven different splice variants that differ widely in subcellular localization, tissue distribution, and ascribed functions. Alternate splicing of the Bin1 gene results in ten transcript variants encoding different isoform. Bin1 is expressed ubiquitously in mammalian cells. Certain splice variants of Bin1 are expressed in the neurons, muscle cells or tumor cells. Bin1 may act with cancer suppressor and inhibits malignant cell transformation. A Study in human tumor cell lines found that most melanoma cells inappropriately expressed exon 12A, suggests that the aberrant splicing of Bin1 may contribute to melanoma progression.
Reference Data

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